This work, which uses Neurospora as an experimental organism, is guided by the working hypothesis that localized increases in the level of calcium in the hyphal cytosol constitute signals for wall extension, and, hence, for the formation and maintenance of growing apices. Evidence in support of this hypothesis is presented in the body of the original proposal, but much work remains to be carried out to verify it and elucidate how the calcium signal is generated, modulated and enforced. By clarifying these questions, we hope to contribute significantly to the old puzzles of apical growth and branching. The proposed methodology will combine the tools of biochemistry, microscopic morphology, physiology and genetics. The last will be used to dissect the morphogenetic circuitry which determines apical growth, and will rely on the available conditional colonial mutants, on revertants thereof and on a hunt for temperature-sensitive mutants deficient in the ability to grow apically. The microscopic methods will use fluorescent probes to correlate calcium reservoirs with cell-wall structure. Biochemistry will be used to monitor calcium fluxes (using 45 Ca) and to investigate target systems (autolysins). N-acetylgalactosaminoglycan deacetylase will also be studied to ascertain whether, as suspected, it is critical in morphogenesis.